Impact of Ultrathin Strut Biodegradable Polymer Sirolimus-Eluting Stents in Percutaneous Coronary Intervention for Hemodialysis Patients

Abstract

Background: Hemodialysis (HD) is associated with adverse cardiovascular events after percutaneous coronary intervention (PCI). Although the ultrathin strut biodegradable polymer sirolimus-eluting stent (ultrathin strut BP-SES) has had better results in patients undergoing PCI compared with other drug-eluting stents (DES), its usefulness in HD patients is unknown.

Methods and Results: This study involved 286 lesions in 162 HD patients who underwent PCI with a DES between January 2018 and June 2022. The incidence of clinically driven target lesion revascularization (TLR), target vessel failure (TVF: cardiac death, target vessel MI and clinically driven target vessel revascularization [TVR]) was assessed. During a median 636 days, clinically driven TLR occurred in 32 lesions. Clinically driven TLR at 2 years was significantly lower in the ultrathin strut BP-SES group than in the other DES group (2.9% vs. 17.3%, log-rank P=0.028). TVF occurred in 43 patients. The cumulative incidence of TVF was not different between two groups; however, clinically driven TVR was significantly lower in patients treated with the ultrathin strut BP-SES than with other DES (4.5% vs. 25.7%, log-rank P=0.027). In the quantitative coronary angiography analysis, late lumen loss at follow-up was significantly smaller in the ultrathin strut BP-SES group (0.13±0.40 vs. 0.67±1.02 mm, P<0.001).

Conclusions: In patients on HD undergoing PCI, the incidence of clinically driven TLR was significantly lower in ultrathin strut BP-SES compared to other DES.

The cardiovascular mortality rate in patients on hemodialysis (HD) is estimated to be 10–20-fold higher than that for individuals without chronic kidney disease.¹ Coronary artery lesions in patients on HD often have severe vascular calcification, which is strongly associated with adverse cardiovascular events.² HD independently predicts a worse outcome for ischemia-driven target lesion revascularization (TLR) in the early phase after percutaneous coronary intervention (PCI).³ Although 2nd-generation drug-eluting stents (DES) have improved clinical outcomes after PCI compared with the 1st-generation DES, major adverse events after PCI with 2nd-generation DES occur more frequently in patients on HD than in those not on HD.¹ HD remains an independent predictor of TLR even after the implantation of 2nd-generation DES.³

Several randomized clinical trials have shown that the sirolimus-eluting stent with a biodegradable polymer and ultrathin strut (ultrathin strut BP-SES; Orsiro, Biotronik, Bülach, Switzerland) has a lower target lesion failure rate at 1 year after PCI compared with other 2nd-generation DES.^4,5 Furthermore, in patients with acute ST-elevation myocardial infarction, primary PCI using the ultrathin strut BP-SES proved superior to conventional stent types.⁶ However, patients on HD were often excluded from these randomized controlled trials, or only a limited number of patients on HD are included.^5,6 Therefore, because the effectiveness of the ultrathin strut BP-SES in PCI for patients on HD remains unclear, we compared the clinical outcomes of PCI in patients on HD treated with the ultrathin strut BP-SES vs. those treated with other types of DES.

Methods

Study Design and Population

This study was a single-center, retrospective study. Between January 2018 and June 2022, 286 lesions in 162 patients on HD were successfully treated with PCI using DES at Kurashiki Central Hospital. After excluding 11 lesions treated with hybrid stenting (involving different types of DES), a total of 275 lesions in 156 patients were included in this study. There were 46 lesions in 27 patients treated with the ultrathin strut BP-SES and 229 lesions in 129 patients treated with other types of 2nd-generation DES (stent details are given in Table 1).

Table 1.

Patients’ Characteristics

	Overall (N=156)	Ultrathin strut BP-SES (N=27)	Other DES (N=129)	P value*
Clinical characteristics
Age (years)	71.7±10.3	73.4±8.6	71.4±10.7	0.35
>75 years	69 (44.2)	12 (44.4)	57 (44.2)	0.98
Male	119 (76.3)	19 (70.4)	100 (77.5)	0.43
Hypertension	128 (82.1)	21 (77.8)	107 (82.9)	0.53
Diabetes mellitus	99 (63.5)	14 (51.9)	85 (65.9)	0.17
Use of insulin	30 (19.2)	2 (7.4)	28 (21.7)	0.09
Dyslipidemia	93 (5.96)	14 (51.9)	79 (61.2)	0.37
Smoking	87 (55.8)	13 (48.1)	74 (57.4)	0.38
Peripheral vascular disease	46 (29.5)	8 (29.6)	38 (29.5)	0.99
Prior myocardial infarction	45 (28.8)	7 (25.9)	38 (29.5)	0.71
Prior coronary revascularization	69 (44.2)	10 (37.0)	59 (45.7)	0.41
Left ventricular ejection fraction (%)	48.9±11.7	48.4±12.9	48.9±11.5	0.82
Medications at hospital discharge
Statin	111 (71.2)	25 (92.6)	86 (66.7)	0.007
ACE-I/ARB	54 (34.6)	12 (44.4)	42 (32.6)	0.24
β-blocker	95 (60.9)	14 (51.9)	81 (62.8)	0.29
Antihyperphosphatemia drug	110 (70.5)	18 (66.7)	92 (71.3)	0.63
Antithrombotic therapy
Aspirin	149 (95.5)	25 (92.6)	124 (96.1)	0.42
Clopidogrel	69 (44.2)	13 (48.1)	56 (43.4)	0.82
Prasugrel	85 (54.5)	14 (51.9)	71 (55.0)	0.76
Warfarin	11 (7.1)	1 (3.8)	10 (7.8)	0.48

Categorical data are reported as number and percentage and compared using the chi-square test or Fisher’s exact test. Continuous data are reported as the mean and standard deviation and compared using Student’s t-test. *P values were calculated between patients with and without BP-SES. ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker; BP-SES, biodegradable polymer sirolimus-eluting stent; DES, drug-eluting stent.

This study was approved by the Institutional Committee on Human Research at Kurashiki Central Hospital. The study was conducted in accordance with the provisions of the Declaration of Helsinki and the guidelines for epidemiological studies issued by the Ministry of Health, Labour and Welfare of Japan. All patients provided informed consent for the procedure and subsequent data collection.

Procedural Details and Follow-up

The choice of PCI strategy, including approach site, balloon catheter and type of DES, was at the discretion of each operator. However, all lesions were treated under the guidance of intravascular imaging using either intravascular ultrasound (IVUS) or optical coherence tomography (OCT). Before PCI, loading doses of aspirin (200 mg) and either clopidogrel (300 mg) or prasugrel (20 mg) were administered unless patients had previously received antiplatelet therapy. The antiplatelet therapy after PCI was determined according to the current guidelines.⁷ In most cases patients were treated with dual antiplatelet therapy (aspirin and a P2Y12 receptor antagonist) for 3 months, followed by lifelong single antiplatelet therapy, primarily using a P2Y12 receptor antagonist.⁸ If patients required anticoagulation therapy, they were given dual antiplatelet therapy, along with anticoagulant therapy, in the hospital, and continued with single antiplatelet therapy plus anticoagulant therapy for 1 year, after which only anticoagulant therapy was maintained.⁷

Clinical Follow-up and Study Endpoints

Clinical follow-up was conducted through on-site visits for 3 months and then annually after PCI. If patients were unable to attend follow-up appointments, telephone interviews were conducted with them, their family members, or their family physicians to collect information on survival status and clinical events. The primary outcome of this study was the incidence of clinically driven TLR at 2 years, and the secondary outcome was target vessel failure (TVF), all-cause death, definite stent thrombosis (ST), any TLR (all lesions and non-ostial lesions) at 2 years post-PCI. TVF was defined as a composite of cardiac death (CD), target vessel myocardial infarction (TVMI, including procedural MI) and clinically driven target vessel revascularization (TVR). We assessed the occurrence of TLR and ST in each lesion, and TVF and all-cause death in each patient. Procedural infarction was defined as CK-MB level ≥10-fold the upper limit of normal, with or without new abnormal Q-waves on ECG recorded the day after PCI was performed.⁹ In this study, we defined ST according to the Academic Research Consortium.¹⁰

Angiographic and Intravascular Imaging

Follow-up coronary angiography (CAG) was scheduled for 8 months after PCI if requested by the patient. Quantitative CAG (QCA) analysis was performed using QCA-CMS from Medis Medical Imaging Systems (Leiden, The Netherlands).¹¹ The angiograms were analyzed in random order by 2 experienced observers who were blinded to the patients’ clinical characteristics. Angiographic measurements were taken from multiple angles after intracoronary nitrate injection. Reference diameter, minimum lumen diameter (MLD), diameter stenosis and lesion length were measured on periprocedural and follow-up angiograms. Acute gain was defined as the difference between the preprocedural and postprocedural MLD, and late lumen loss was defined as the difference between postprocedural MLD and MLD at follow-up.

Calcified nodules were defined by intravascular imaging: IVUS or OCT. The characteristics of a calcified nodule on IVUS were defined as a convex shape of calcium on the luminal side and an irregular leading edge of calcium.¹² The characteristics of a calcified nodule in OCT were defined as calcified plaque with fibrosis cap disruption.¹³

Statistical Analysis

Continuous variables are expressed as mean±standard deviation or median (interquartile range) and compared using unpaired Student’s t-test or Mann-Whitney U test. Categorical variables are expressed as numbers and percentages and compared using the chi-square test or Fisher’s exact test. Time-to-first-event curves were generated using the Kaplan-Meier method and compared using the log-rank test. A multivariable Cox proportional hazards model was developed to assess the effect of the ultrathin strut BP-SES, adjusting for the following potential confounders: age, sex, hypertension, diabetes treated with insulin, and dyslipidemia. All reported P values are two-sided, and P<0.05 was considered statistically significant. All analyses were conducted using IBM SPSS Statistics software, version 27.0 (IBM Corp., New York, NY, USA).

Results

Patients’ and Lesion Characteristics

Baseline patient characteristics are summarized in Table 1. The mean age was 71.7±10.3 years, and 76.3% of the patients were male. The prevalence of coronary artery risk factors, including hypertension, diabetes mellitus, dyslipidemia and smoking, did not differ between the ultrathin strut BP-SES and non-ultrathin strut BP-SES groups. Statins were more frequently used in the ultrathin strut BP-SES group. Table 2 shows the characteristics of the lesions and procedures. The percentage of cases in which the left circumflex artery was the target vessel was significantly higher in the ultrathin strut BP-SES group than in the non-ultrathin strut BP-SES group. The prevalence of ostial lesions was higher in the non-ultrathin strut BP-SES group. The size of the implanted stent was significantly smaller in the ultrathin strut BP-SES group.

Table 2.

Lesion and Procedural Characteristics

	Overall (N=275)	Ultrathin strut BP-SES (N=46)	Other DES (N=229)	P value*
Lesion characteristics
Acute coronary syndrome	67 (24.4)	10 (21.7)	57 (24.9)	0.65
STEMI	29 (10.5)	4 (8.7)	25 (10.9)	0.79
NSTEMI	38 (13.8)	6 (13.0)	32 (14.0)	0.87
Target vessel				0.06
LMT	4 (1.4)	0 (0)	4 (1.7)
LAD	96 (34.9)	14 (30.4)	82 (35.8)
LCX	54 (19.6)	16 (34.8)	38 (16.6)
RCA	116 (42.2)	16 (34.8)	100 (43.7)
SVG graft	5 (1.8)	0 (0)	5 (2.2)
Bifurcation lesion	74 (26.9)	11 (23.9)	63 (27.5)	0.62
Calcified nodule	97 (35.3)	17 (37.0)	80 (34.9)	0.79
CTO	16 (5.8)	2 (4.3)	14 (6.1)	1.00
Ostial lesion	30 (10.9)	0 (0)	30 (13.1)	0.009
Procedural characteristics
Intravascular imaging	275 (100)	46 (100)	229 (100)	1.00
IVUS	244 (88.7)	39 (84.8)	205 (89.5)	0.35
OCT	31 (11.3)	7 (15.2)	24 (10.5)	0.35
Atherectomy device
Rota	40 (14.5)	10 (21.7)	30 (13.1)	0.13
OAS	9 (3.3)	3 (6.5)	6 (2.6)	0.18
Stent
Number	1.09±0.30	1.07±0.25	1.09±0.30	0.58
Size (mm)	3.07±0.58	2.88±0.51	3.11±0.58	0.01
Length (mm)	26.9±13.1	24.7±11.0	27.2±13.5	0.50
Max. balloon pressure (atm)	20.0±5.8	19.5±6.4	20.1±5.7	0.57
Stent type (other DES group)
DP-EES			111
U-SES			44
BP-EES			38
R-ZES			30
Others			6

Categorical data are reported as number and percentage and compared using the chi-square test or Fisher’s exact test. Continuous data are reported as the mean and standard deviation and compared using Student’s t-test. *P values were calculated between patients with and without BP-SES. ACS, acute coronary syndrome; BP-SES, biodegradable polymer sirolimus-eluting stent; CTO, chronic total occlusion; DES, drug-eluting stent; IVUS, intravascular ultrasound; LAD, left ascending artery; LCX, left circumflex artery; LMT, left main trunk; NSTEMI, non-ST-elevation myocardial infarction; OCT, optical coherence tomography; RCA, right coronary artery; STEMI, ST-elevation myocardial infarction.

2-Year Clinical Outcomes

During a median follow-up of 636 days (interquartile range 241–730 days), clinically driven TLR occurred in 32 lesions, and the cumulative incidence of clinically driven TLR was significantly lower in the ultrathin strut BP-SES group compared with the non-ultrathin strut BP-SES group (2.9% vs. 17.3%, log-rank P=0.028; Figure 1). TVF occurred in 43 patients, and the cumulative incidence of TVF at 2 years did not differ between groups (18.7% vs. 32.4%, log-rank P=0.242, Figure 2A). Regarding TVF, the cumulative incidences of CD and TVMI were no different between groups (CD: 15.0% vs. 10.2%, log-rank P=0.427, Figure 2B; TVMI: 3.7% vs. 10.6%, log-rank P=0.345, Figure 2C). However, the cumulative incidence of clinically driven TVR was lower in the patients treated with the ultrathin strut BP-SES group compared with those treated with other types of 2nd-generation DES (4.5% vs. 25.7%, log-rank P=0.027, Figure 2D). The 2-year cumulative incidences of any TLR (all lesions), any TLR (non-ostial lesions), all-cause death and ST are shown in Table 3.

Figure 1.

Kaplan-Meier curves of cumulative incidence of clinically driven target lesion revascularization (TLR) at 2 years after PCI between the ultrathin strut BP-SES group and the non-ultrathin strut BP-SES group. BP-SES, biodegradable polymer sirolimus-eluting stent; PCI, percutaneous coronary intervention.

Figure 2.

Kaplan-Meier curves of target vessel failure (TVF) at 2 years after PCI between the ultrathin strut BP-SES group and the non-ultrathin strut BP-SES group. Cumulative incidence of (A) target vessel failure, (B) cardiac death, (C) target vessel myocardial infarction and (D) clinically driven target vessel revascularization. BP-SES, biodegradable polymer sirolimus-eluting stent; PCI, percutaneous coronary intervention.

Table 3.

Primary and Secondary Outcomes

	Ultrathin strut BP-SES	Other DES	P value*
Primary outcome
Clinically driven TLR	1 (3.3)	31 (17.3)	0.028
Secondary outcomes
TVF	5 (18.7)	38 (32.4)	0.24
CD	4 (15.0)	12 (10.2)	0.43
Clinically driven TVR	1 (4.5)	28 (25.7)	0.027
TVMI	1 (3.7)	12 (10.6)	0.35
All-cause death	6 (22.2)	37 (29.7)	0.52
Definite ST	0 (0.0)	1 (0.5)	0.66
Any TLR (all lesions)	1 (3.3)	40 (22.7)	0.006
Any TLR (non-ostial lesions)	1 (3.3)	32 (20.7)	0.013

BP-SES, biodegradable polymer sirolimus-eluting stent; CD, cardiac death; DES, drug-eluting stent; ST, stent thrombosis; TLR. target lesion revascularization; TVF, target vessel failure; TVMI, target vessel myocardial infarction.

Figure 3 presents the hazard ratios (HR) and 95% confidence intervals (CI) from the Cox proportional hazards model, adjusted for patient and procedural characteristics. PCI with the ultrathin strut BP-SES was independent prognostic factor of clinically driven TLR (HR 0.14, 95% CI 0.02–1.00, P=0.05).

Figure 3.

Cox proportional hazard model of clinically driven TLR adjusted by patient and lesion characteristics. BP-SES, biodegradable polymer sirolimus-eluting stent; CI, confidence interval; HR, hazard ratio.

QCA Findings

The QCA findings from PCI and follow-up are presented in Table 4. There was no significant difference in acute gain or diameter stenosis before and after PCI between groups. However, the pre- and postprocedural MLD was significantly smaller in the ultrathin strut BP-SES group than in the non-ultrathin strut BP-SES group. QCA analysis was performed on 115 lesions during follow-up angiography. Although MLD at follow-up did not differ between groups, diameter stenosis and late lumen loss were significantly smaller in the ultrathin strut BP-SES group than in the non-ultrathin strut BP-SES group (late lumen loss: 0.13±0.40 vs. 0.67±1.02 mm, P<0.001).

Table 4.

Quantitative Coronary Angiography Findings

	Overall (N=226)	Ultrathin strut BP-SES (N=37)	Other DES (N=189)	P value*
At procedure
Baseline RD (mm)	3.04±0.05	2.85±0.63	3.08±0.74	0.07
Baseline MLD (mm)	0.99±0.04	0.80±0.59	1.02±0.54	0.03
MLD after PCI (mm)	2.80±0.04	2.63±0.57	2.83±0.55	0.04
Baseline diameter stenosis (%)	68.1±1.16	72.0±19.8	67.3±16.9	0.14
Diameter stenosis post-PCI (%)	13.9±0.56	14.6±8.41	13.8±8.51	0.62
Baseline lesion length (mm)	19.4±0.78	20.0±9.78	19.3±11.8	0.74
Acute gain (mm)	1.81±0.04	1.83±0.75	1.81±0.62	0.91
	(N=115)	(N=16)	(N=99)	P value*
At follow-up
RD (mm)	2.89±0.10	2.88±0.49	2.89±1.10	0.94
MLD (mm)	2.18±0.09	2.38±0.41	2.15±1.00	0.10
Diameter stenosis (%)	30.2±2.51	16.6±9.05	32.4±28.3	<0.01
Late lumen loss (mm)	0.59±0.09	0.13±0.40	0.67±1.02	<0.01

Continuous data are reported as mean and standard deviation and compared using Student’s t-test. *P values were calculated between patients with and without BP-SES. BP-SES, biodegradable polymer sirolimus-eluting stent; DES, drug-eluting stent; MLD, minimal lumen diameter; PCI, percutaneous coronary intervention; RD, reference diameter.

Discussion

The following are the main findings of the present study. (1) In patients on HD undergoing PCI, the ultrathin strut BP-SES was associated with lower rates of clinically driven TLR and clinically driven TVR at 2 years after PCI compared with other DES. (2) Late lumen loss on follow-up CAG was significantly lower in the ultrathin strut BP-SES group than in the non-ultrathin strut BP-SES group. This is the first study to investigate the effect of the ultrathin strut BP-SES on lower stent-related adverse events and late lumen loss at follow-up in patients on HD.

The main features of this stent type are the ultrathin struts (60 μm [≤3.0-mm stents] or 80 μm [>3.0-mm stents]), a passive coating of amorphous silicon carbide, and a biodegradable coating of eluting sirolimus.¹⁴ In previous studies, PCI with other types of DES for patients on HD had a poor prognosis following treatment,^15,16 one reason being severe calcification, including calcified nodules, which often causes in-stent restenosis (ISR) in patients on HD.¹⁷ The mechanism of calcified nodular formation following DES implantation has 3 phases. In the early phase, fibrin with calcification forms a calcified nodule. In the middle phase, calcium fragmentation and fibrin deposition, caused by sheet calcium destruction under mechanical stress, form calcified nodules. In the late phase, over several years, a possible mechanism for the development of neoatherosclerosis is the formation of new calcified nodules; however, the detailed mechanism is unknown.¹⁸ The early- and middle-phase mechanisms are considered to be associated with midterm ISR. Because high platelet reactivity has been reported in patients on HD,¹⁹ thrombosis following stent implantation is more common in HD than in non-HD patients.²⁰ The amorphous silicon carbide coating of the ultrathin strut BP-SES inhibits the release of metal ions from the stent, which is involved in fibrinogen-to-fibrin conversion and thrombus formation.²¹ This mechanism is potentially one of the factors contributing to the reduction in calcified nodular formation in the early phase following ultrathin strut BP-SES implantation. Severe calcification and nodular calcification delay stent strut coverage,^22,23 which can result in ST. In a previous study that used OCT, earlier stent coverage was noted in lesions treated with the ultrathin strut BP-SES compared with those treated with durable polymer (DP) everolimus-eluting stents.²⁴ That finding supports the antithrombotic effect of the ultrathin strut BP-SES. Furthermore, thinner struts may prevent midterm calcified nodular formation by reducing the mechanical stress.

In patients on HD, a small MLD is also an independent risk factor for ISR following DES implantation.¹⁷ In small vessels, thinner stents are reportedly associated with lower rates of restenosis.²⁵ Therefore, the ultrathin strut BP-SES may be more advantageous than other DES in lesions with a small MLD.

In this study, the rate of calcified nodule lesions was approximately 30% between the groups, and the MLD before PCI was considerably smaller in the ultrathin strut BP-SES group than in the other group. In both calcified and small vessel lesions, the ultrathin strut tended to decrease the target lesion failure rate compared with the DP-SES used in a previous study.²⁶ The results of our study may extend previous findings to patients on HD.

Two types of ultrathin strut BP-SES are currently available, namely, Orsiro and Ultimaster. In a previous study, the TLR rate in lesions treated with the Ultimaster was 19.2% in patients on HD.²⁷ The Orsiro has an ultrathin strut and a passive coating of amorphous silicon carbide, whereas the Ultimaster does not, which could be the reason why the TLR rates of the ultrathin strut BP-SES were lower than those of other DES, including the Ultimaster.

In a previous study, the rates of major adverse cardiac events were substantially lower in lesions treated with paclitaxel-eluting stents than in those treated with sirolimus-eluting stents,²⁸ but in another long-term study, the rates of major adverse cardiac events were similar for both types of stent.²⁹ Therefore, the most effective eluting drug for patients on HD is unclear.

Study Limitations

First, this was a single-center, retrospective, observational study. The selection of treatment strategies, including the stent type, was not randomized and relied on the operator’s discretion. A selection bias in the treatment strategy might have influenced our study results. Second, the number of patients treated with ultrathin strut BP-SES was smaller than that of patients treated with other DES. Therefore, further studies that include a larger number of patients are warranted. Third, patients treated with the ultrathin strut BP-SES often took statins at hospital discharge. In a previous study, HD patients taking statins had a significantly lower rate of major adverse cardiac events.³⁰ In this study, multivariate analysis including statins revealed that the ultrathin strut BP-SES was significantly associated with a lower TLR rate; however, this result may have been influenced by the higher statin intake in the ultrathin strut BP-SES group.

Conclusions

In patients on HD undergoing PCI, the incidence of clinically driven TLR was significantly lower when treated with the ultrathin strut BP-SES compared with other DES.

Funding

None.

Acknowledgment

The authors are grateful for the contributions of all the investigators.

Disclosures

All authors have no conflicts of interest directly relevant to the content of this article.

IRB Information

Approved by the Ethics Review Board of Kurashiki Central Hospital. Reference number: 4290.

Data Availability

The data, analytic methods, and study materials will not be made available to other researchers for purposes of reproducing the results or replicating the procedure.

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